Search

Background: A virus infection may lead the body to produce more immune cells of particular types or stimulate the production of new ones, both of which may have anti-leukemic effects. There has been no research on whether immune cells stimulated by varicella-zoster virus (VZV) infection have anti-leukemic effects. The objective of this investigation is to assess the impact of VZV infection on patients' long-term survival following allogeneic hematopoietic stem cell transplantation (allo-HSCT). Methods: This retrospective study investigated the association between varicella-zoster virus (VZV) reactivation and outcomes in 219 individuals who received allogeneic hematopoietic stem cell transplantation (allo-HSCT) at the Sun Yat-sen University's First Affiliated Hospital. According to being diagnosed with VZV infection or not, these patients were grouped into two groups. The comparison of cumulative incidence of relapse, non-recurrent mortality, and overall survival (OS) was conducted between the two groups. Results: Analyzing multivariate data, VZV reactivation was linked to lower relapse incidence in the group containing all individuals (hazard ratio [HR] = 0.27; 95% confidence interval [CI], 0.12–0.64), patients suffering from acute myeloid leukaemia (HR = 0.10; 95% CI, 0.01–0.83), and patients suffering from acute lymphoblastic leukaemia (HR = 0.25; 95% CI, 0.08–0.77). Moreover, VZV reactivation was linked with decreased non-relapse mortality in all individuals (HR = 0.20; 95% CI, 0.05–0.79), but no statistical significance was found for any disease subgroup. Further, VZV reactivation was an independent predictor for improved OS in the group containing all individuals (HR = 0.10; 95% CI, 0.03–0.29), patients suffering from acute myeloid leukaemia (HR = 0.09; 95% CI, 0.01–0.66), and patients suffering from acute lymphoblastic leukaemia (HR = 0.16; 95% CI, 0.04–0.68). Conclusion: This is the first study to show that VZV reactivation following allo-HSCT is an independent predictor for lower relapse rates and improved OS, providing novel therapeutic approaches to improve patients' long-term survival following allo-HSCT. [ABSTRACT FROM AUTHOR]

The Blattulidae Vishniakova, 1982 is an extinct family of cockroaches which was widely distributed around the world from Late Triassic to Late Cretaceous. Huablattula vrsanskyi sp. n., based on a well-preserved specimen from mid-Cretaceous Kachin amber differs from other species of genus Huablattula Qiu et al., 2019 in having different patterns on the pronotum, forewing with vein A bifurcated and hind wing without pterostigma. The new discovery enriched the diversity of the family Blattulidae in Kachin amber and expanded our understanding of cockroach structure and phylogeny. [ABSTRACT FROM AUTHOR]

Sorptive removal of hexavalent chromium (Cr(VI)) bears the advantages of simple operation and easy construction. Customized polymeric materials are the attracting adsorbents due to their selectivity, chemical and mechanical stabilities. The mostly investigated polymeric materials for removing Cr(VI) were reviewed in this work. Assembling of robust functional groups, reduction of self-aggregation, and enhancement of stability and mechanical strength, were the general strategies to improve the performance of polymeric adsorbents. The maximum adsorption capacities of these polymers toward Cr(VI) fitted by Langmuir isotherm model ranged from 3.2 to 1185 mg/g. Mechanisms of complexation, chelation, reduction, electrostatic attraction, anion exchange, and hydrogen bonding were involved in the Cr(VI) removal. Influence factors on Cr(VI) removal were itemized. Polymeric adsorbents performed much better in the strong acidic pH range (e.g., pH 2.0) and at higher initial Cr(VI) concentrations. The adsorption of Cr(VI) was an endothermic reaction, and higher reaction temperature favored more robust adsorption. Anions inhibited the removal of Cr(VI) through competitive adsorption, while that was barely affected by cations. Factors that affected the regeneration of these adsorbents were summarized. To realize the goal of industrial application and environmental protection, removal of the Cr(VI) accompanied by its detoxication through reduction is highly encouraged. Moreover, development of adsorbents with strong regeneration ability and low cost, which are robust for removing Cr(VI) at trace levels and a wider pH range, should also be an eternally immutable subject in the future. Work done will be helpful for developing more robust polymeric adsorbents and for promoting the treatment of Cr(VI)-containing wastewater. [ABSTRACT FROM AUTHOR]

[Display omitted] • Fe-C micro-electrolysis modified by H 2 O 2 was first used for treating Cr(pic) 3. • No Cr(VI) was accumulated. • Continuous treatment of Cr(pic) 3 was realized. • The modified process consumed less H 2 O 2 than the Fenton process. • The method exhibited strong stability in various water matrixes. Cr(pic) 3 , an emerging contaminant, is easily degraded to hexavalent chromium (Cr(VI)) in environment, which exacerbates its risk. Because of the complexing structure, removal of this organic chromium is rather difficult through the simple adsorption and precipitation. Herein, disposal of Cr(pic) 3 via the modified iron-carbon (Fe-C) micro-electrolysis (abbreviated as Fe-C) process (H 2 O 2 was added simultaneously as the reactant) was first developed in this work. The modified process could accelerate the de-complexation of Cr(pic) 3 and promote Cr removal at a lower H 2 O 2 dosage than the Fenton process. Cr(VI) was not accumulated in the process. Almost all the Cr(pic) 3 could be degraded and the residual chromium (all was trivalent chromium Cr(III)) was decreased from 520 to 52.7 μg/L within 30 min under optimized conditions in batch experiments (i.e., pH initial = 3.0, pH final = 7.0, [H 2 O 2 ] 0 = 0.3 mM, [Fe-C fillers] 0 = 0.1 g/L, respectively). Mechanisms of Cr(pic) 3 de-complexation and Cr removal were elucidated based on the products detected and characteristics of the precipitates. Adsorption was the main mechanism for Cr(III) removal. It exchanged the hydroxyl ligand with the iron hydro(oxides) to form inner sphere complex. Factors that potentially affected the performance of the modified Fe-C process were investigated, including the operational parameters and the composition of water matrix. Moreover, the feasibility and stability of the established method were further confirmed by the column test, which realized the continuous operation and maintained the residual Cr in the effluent constant below 10.0 μg/L. Collectively, these findings consistently indicated that the modified Fe-C process is a robust and promising approach for the industrial disposal of Cr(pic) 3. [ABSTRACT FROM AUTHOR]

Forest ecosystem is the most important terrestrial ecosystem type of species diversity in the world. The protection and sustainable use of forest ecological diversity is of great significance to forest protection and sustainable management. In order to maintain biodiversity, the traditional concept of forest resources management must be changed. In recent years, the mining and application of big data have become the frontier content of international ecological diversity and macroecology research. By establishing the discrete dynamic model of forest ecological diversity change, this study finds a method that can keep the number of trees stable in a short time and ensure the sustainable development of forest resources. This article studies and constructs the forest information system and constructs an open-source WebGIS (network geographic information system) scheme for the field of spatial information and supporting OGC (occupationally generated content). At the same time, the grey theory GM (1,1) model is used to predict the development trend of forest resources in China. The results show that under the promotion of policies and research projects, China's forestry development has realized the double growth of forest area and volume, and the forest coverage rate has reached a new level. [ABSTRACT FROM AUTHOR]

Background: Immunosurveillance is pivotal in the effectiveness of anticancer therapies and tumor control. The ineffectiveness of cisplatin in activating the immunosurveillance is attributed to its lack of adjuvanticity resulting from its inability to stimulate endoplasmic reticulum stress. Dihydroartemisinin demonstrates the anti-tumor effects through various mechanisms, including the activation of the endoplasmic reticulum stress. This study aimed to develop a novel strategy to enhance the immunogenicity of dying tumor cells by combining cisplatin with dihydroartemisinin, thereby triggering effective anti-tumor immunosurveillance and improving the efficacy of cisplatin in clinical practice. Methods: Lewis lung carcinoma (LLC) and CT26 colon cancer cell lines and subcutaneous tumor models were used in this study. The importance of immunosurveillance was validated in both immunocompetent and immunodeficient mouse models. The ability of dihydroartemisinin and cisplatin therapy to induce immunogenic cell death and tumor growth control in vivo was validated by prophylactic tumor vaccination and therapeutic tumor models. The underlying mechanism was elucidated through the pharmaceutical or genetic intervention of the PERK/eIF2α pathway in vitro and in vivo. Results: Dihydroartemisinin enhanced the generation of reactive oxygen species in cisplatin-treated LLC and CT26 cancer cells. The combination treatment of dihydroartemisinin with cisplatin promoted cell death and ensured an optimal release of damage-associated molecular patterns from dying cancer cells, promoting the phagocytosis of dendritic cells. In the tumor vaccination model, we confirmed that dihydroartemisinin plus cisplatin treatment induced immunogenic cell death. Utilizing immunocompetent and immunodeficient mouse models, we further demonstrated that the combination treatment suppressed the tumor growth of CT26 colon cancer and LLC lung cancer, leading to an improved prognosis through the restoration of cytotoxic T lymphocyte responses and reinstatement of anti-cancer immunosurveillance in vivo. Mechanistically, dihydroartemisinin restored the immunogenicity of cisplatin by activating the adjuvanticity of damage-associated molecular patterns, such as calreticulin exposure, through the PERK/eIF2α pathway. Additionally, the inhibition of eIF2α phosphorylation attenuated the anti-tumor efficiency of C + D in vivo. Conclusions: We highlighted that dihydroartemisinin acts as an immunogenic cell death rescuer for cisplatin, activating anticancer immunosurveillance in a PERK/eIF2α-dependent manner and offering a strategy to enhance the anti-tumor efficacy of cisplatin in clinical practice. [ABSTRACT FROM AUTHOR]

Cr(VI) compounds are confirmed human carcinogens. Maternally expression 3 (MEG3) is the first long non-coding RNA to be identified as a tumor suppressor. MEG3 is frequently downregulated or lost in various primary human tumor tissues and cancer cell lines. Downregulation of MEG3 is associated with cancer initiation, progression, and metastasis. Our previous study has revealed that MEG3 was lost and NEDD9 was upregulated in Cr(VI)-transformed cells compared to those in passage-matched normal BEAS-2B cells. Overexpression of MEG3 reduced NEDD9. β-Catenin was activated in Cr(VI)-transformed cells, overexpression of MEG3 or knockdown of NEDD9 inhibited the activation of β-Catenin. The results from the present study showed that isorhapontigenin (ISO) treatment is able to suppress cell proliferation, migration, and invasion of Cr(VI)-transformed cells. Further study showed that ISO treatment in Cr(VI)-transformed cells decreases the levels of Ki67, a biomarker for cell proliferation, and of cyclin D1, a regulator for the cell cycle. ISO elevated the MEG3 expression level in Cr(VI)-transformed cells. The DNA methylation transferases DNMT3a, DNMT3b, and DNMT1 levels were reduced upon ISO treatment. ISO treatment decreased both mRNA and protein levels of NEDD9. In addition, ISO treatment reduced the activation of β-catenin. Slug was upregulated and E -Cadherin was downregulated in Cr(VI)-transformed cells, treatment with ISO decreased Slug and increased E -Cadherin. This study demonstrated that ISO is a potent therapeutical agent against lung cancer induced by Cr(VI). • Cr(VI) is a confirmed human carcinogen. • ISO is an orally bioavailable dietary polyphenol. • ISO inhibits proliferation of Cr(VI)-transformed cells. • ISO inhibits of migration and invasion of Cr(VI)-transformed cells. [ABSTRACT FROM AUTHOR]

[Display omitted] • Treatment of Cr(pic) 3 using Fenton process was first proposed. • Decomplexing of Cr(pic) 3 by oxidation facilitated the overall Cr removal. • Simultaneous Cr(pic) 3 oxidation and Cr removal were achieved. • Cr(VI) barely accumulated in aqueous phase. Chromium picolinate (Cr(pic) 3) is widely used for feeding animals. Most Cr(pic) 3 administered to animals is excreted without change. The land use of animal waste introduces Cr(pic) 3 to the environment. Transformation of Cr(pic) 3 in the environment releases hexavalent chromium (Cr(VI)), posing a chromium contamination risk. Because chromium (in trivalent valent) is complexed by picolinic acid (pic), removal of chromium in Cr(pic) 3 form via direct adsorption and precipitation methods is rather difficult. Release of chromium from Cr(pic) 3 first and then removal of it through the combination of adsorption and precipitation is advisable. To this end, the treatment of Cr(pic) 3 using the Fenton process was first investigated in this work. Treatment parameters were optimized for Cr(pic) 3 degradation and chromium removal (i.e., initial and final pH of 3.0 and 7.0, and the molar ratio of Fe(II) and H 2 O 2 was 1:2). Adverse effects of the water constituents could be mitigated by flexible adjustment of the Fenton reagent dosages and the external addition of iron ions. The residual chromium in the aqueous phase was simultaneously lowered to the required standard, and Cr(VI) was barely detected in the aqueous phase. Mechanisms of Cr(pic) 3 degradation and chromium removal were proposed by the intermediates determined. The results obtained indicate that the Fenton process is robust for degrading Cr(pic) 3 and removing chromium simultaneously and is promising for treating Cr(pic) 3 -containing wastewater. [ABSTRACT FROM AUTHOR]

Phenylarsonics are present as additives in animal feed in some countries. As only a small fraction of these additives is metabolized in animals, they mostly end up in the environment. A comprehensive investigation of the fate of these additives is crucial for evaluating their risks. This review aims to provide a clear understanding of the transformation mechanism of phenylarsonics in vivo and in vitro and to evaluate their fate and associated risks. Degradation of phenylarsonics releases toxic As species (mainly as inorganic arsenic (iAs)). Trivalent phenylarsonics are the metabolites or biotic degradation intermediates of phenylarsonics. The cleavage of As groups from trivalent phenylarsonics catalyzed by C-As lyase or other unknown pathways generates arsenite (As(III)). As(III) can be further oxidized to arsenate (As(V)) and methylated to methyl-arsenic species. The half-lives associated with abiotic degradation of phenylarsonics ranged from a few minutes to tens of hours, while those associated with biotic degradation ranged from several days to hundreds of days. Abiotic degradation resulted in a higher yield of iAs than biotic degradation. The use of phenylarsonics led to elevated total As and iAs levels in animal products and environmental matrices, resulting in As exposure risk to humans. The oxidation of phenylarsonics to As(V) facilitated the sorptive removal of As, which provides a general approach for treating these compounds. This review provides solid evidence that the use of phenylarsonics has adverse effects on both human health and environmental safety, and therefore, supports their withdrawal from the global market. [Display omitted] • The majority of phenylarsonic end up in the environment. • Metabolization/degradation of phenylarsonic release toxic arsenic species. • Abiotic degradation of phenylarsonic is faster than biotic degradation. • The use of phenylarsonic brings additional arsenic exposure risk to humans. • Oxidation of phenylarsonic to As(V) favors arsenic removal. [ABSTRACT FROM AUTHOR]

Bisphenols (BPs), benzophenone-type UV filters (BP-type UV filters), triclosan (TCS), and triclocarban (TCC) are endocrine-disrupting chemicals (EDCs) and commonly used in consumer and personal care products. In the present study, seven BPs, eight BP-type UV filters, TCS, and TCC were quantified in 196 paired urine and blood samples collected from young adults in South China. Benzophenone-7 and benzophenone-9 were not detected in all samples, while other target compounds were widely detected in 39%–96% of the urine and 14%–96% of the blood samples, and the median concentrations ranged from <0.02 (specific gravity adjusted: < 0.02) to 2.33 (2.05) ng/mL and <0.01–2.66 ng/mL in the urine and blood samples, respectively. Females had higher levels of most target analytes, and gender-related differences (p < 0.05) were found in the blood levels of benzophenone-2 (females vs. males: 0.84 vs. <0.01 ng/mL), ΣBP (sum of BP-type UV filters; 1.61 vs. 0.98 ng/mL), TCS (3.89 vs. 1.69 ng/mL), and ΣTC (sum of TCS and TCC; 5.77 vs. 3.02 ng/mL). We calculated the portioning of the target compounds between blood and urine (B/U ratios). The B/U ratios of bisphenol F, benzophenone-2, benzophenone-6, 4-hydroxy benzophenone, TCS, and TCC were higher than 1, showing that these analytes have higher enrichment capacities in human blood. To the best of our knowledge, this is the first study to simultaneously analyze the concentrations of BPs, BP-type UV filters, TCS, and TCC in the paired urine and blood samples of young adults in South China. [Display omitted] • First study of urinary and blood BPs, BP-type UV filters, TCS, and TCC levels in Chinese young adults. • Gender-related difference in levels of BP-type UV filters, TCS, and TCC were found. • BPF, BP-2, BP-6, 4-OH-BP, TCS, and TCC have higher enrichment capacity in human blood. [ABSTRACT FROM AUTHOR]

Growth arrest and DNA damage (GADD) 45α is a member of GADD inducible gene family, and is inducible in cell response to oxidative stress. GADD45α upregulation induces MKK4/JNK activation in some published experimental systems. However, we found here that the depletion of GADD45α (GADD45α−/−) in mouse embryonic fibroblasts (MEFs) resulted in an increase in the phosphorylation of MKK4/7, MKK3/6 and consequently specific up-regulated the activation of JNK/p38 and their downstream transcription factors, such as c-Jun and ATF2, in comparison to those in GADD45α+/+ MEFs cell following nickel exposure. This up-regulation of MKK-JNK/p38 pathway in GADD45α−/− cell could be rescued by the reconstitutional expression of HA-GADD45α in GADD45α−/− MEFs, GADD45α−/−(HA-GADD45α). Subsequent studies indicated that GADD45α deletion repressed expression of PP2Cα, the phosphotase of MKK3/6 and MKK4/7, whereas ectopic expression of HA-PP2Cα in GADD45α−/− cells attenuated activation of MKK3/6-p38 and MKK4/7-JNK pathways. Collectively, our results demonstrate a novel function and mechanism responsible for GADD45α regulation of MKK/MAPK pathway, further provides insight into understanding the big picture of GADD45α in the regulation of cellular responses to oxidative stress and environmental carcinogens. [ABSTRACT FROM AUTHOR]

Abstract: Arsenic is a well-documented human carcinogen associated with skin carcinogenesis. Our previous work reveals that arsenite exposure is able to induce cell transformation in mouse epidermal cell JB6 Cl41 through the activation of ERK, rather than JNK pathway. Our current studies further evaluate downstream pathway in low dose arsenite-induced cell transformation in JB6 Cl41 cells. Our results showed that treatment of cells with low dose arsenite induced activation of c-Jun/AP-1 pathway, and ectopic expression of dominant negative mutant of c-Jun (TAM67) blocked arsenite-induced transformation. Furthermore, our data indicated that cyclin D1 was an important downstream molecule involved in c-Jun/AP-1-mediated cell transformation upon low dose arsenite exposure, because inhibition of cyclin D1 expression by its specific siRNA in the JB6 Cl41 cells resulted in impairment of anchorage-independent growth of cells induced by low dose arsenite. Collectively, our results demonstrate that c-Jun/AP-1-mediated cyclin D1 expression is at least one of the key events implicated in cell transformation upon low dose arsenite exposure. [Copyright &y& Elsevier]

Abstract: Fe-doped titanium dioxide (TiO2) microspheres with special core–shell structure were prepared by a simple hydro-alcohol thermal method. The morphology and microstructural characteristics of Fe-doped titania microspheres with different Fe3+ doping concentrations were characterized by means of BET, TEM, SEM, XPS, UV–vis DRS, PLS and XRD. The Fe3+ doped TiO2 samples showed the best photocatalytic activity, which were much superior to P25 under both visible and ultraviolet light irradiations. The concentration of Fe3+ was found playing a key role in the photocatalytic degradation of phenol, moreover, 0.5mol% Fe3+ doping was an optimal amount. The probable mechanism was proposed: it was presumed that doping Fe3+ ions into TiO2 structure may overlap the conduction band of TiO2 and the d orbital of Fe3+, which leads to the marked narrowing of the band gap and the extension of visible light response. Meanwhile, since the Fe3+/Fe2+ energy level was just lower than the conduction band of TiO2 while the Fe3+/Fe4+ energy level was slightly above the valence band of TiO2, the Fe3+ dopant can not only play as a temporary trapping sites of photo-induced electrons but can also act as shallow capturing sites of photo-induced holes, which will efficiently separate the photoexcited electrons and holes, prolong the lifetime and at last improve the photocatalytic activity. The superior activity of Fe3+–TiO2 photocatalysts can also be ascribed to the special core–shell structure with high surface area, mesoporous pore and well-crystallized anatase phase. [Copyright &y& Elsevier]

Abstract: The twist-like helix W,N-codoped TiO2 photocatalysts were prepared by a simple one-pot synthesis route to hydrolysis of titania tetrachloride using ammonium tungstate as tungsten and nitrogen sources. The morphology and microstructure characteristics of W,N-codoped titania photocatalysts with different amount of tungsten doping were characterized by means of BET, TEM, SEM, XPS, UV–vis DRS, PLS and XRD. The probable mechanism of codoping effect is proposed. It is presumed that cooperation of nitrogen and tungsten ions leads to produce new states and narrow the band gap between the valence band and conduction band effectively, which will greatly improve the photocatalytic activity in the visible light region. On the other hand, the tungsten ions with changing valences in the W,N-TiO2 samples are considered to act as trapping sites, which will effectively decrease the recombination rate of photo-induced electrons and holes and then increase the photo-oxidation efficiency of the catalysts. The metal and nonmetal codoped 1%-W,N-TiO2 sample shows the best photocatalytic activity, which is much superior to P25 under both visible and ultraviolet light irradiation. The superior activity of W,N-TiO2 photocatalysts can also be ascribed to the special twist-like helix structure with regular holes on the wall, high surface area, large pore volume and well-crystallized anatase phase. [Copyright &y& Elsevier]

Abstract: Arsenite has been well-proved to act as both an environmental carcinogen as well as a tumor therapeutic agent. AP-1 is one of the transcription factors that can be induced upon arsenite stimulation. However, the study on the mechanism and the function of the arsenite-induced AP-1 transactivation remains far complete. Here we demonstrated that high dose of arsenite induced apoptotic response in mouse fibroblasts correlating with AP-1 transactivation, which events were mediated by both IKKα and IKKβ, two major protein kinases responsible for NF-κB activation. In addition, the regulatory effect of IKKs on the arsenite-induced AP-1 activation was delivered by sequential induction of GADD45α expression and the activation of MAPKK (MKK3/4/6) and MAPK (JNK and p38K)-dependent pathways. We further provided evidence that p50, but not p65 subunit of NF-κB, was involved in GADD45α induction and the subsequent MAPKK/MAPK/AP-1 activation under arsenite exposure, while functional NF-κB induced by arsenite stimulation consisted of p65 but not of p50 subunit. Therefore, we concluded that both IKKα and IKKβ can mediate arsenite-induced AP-1 transactivation through NF-κB activity-independent manner. [Copyright &y& Elsevier]

Abstract: Novel self-assembled Mg5(CO3)4(OH)2 ·4H2O with nanosheet structure was fabricated through simple hydrothermal method without any templates. Series of MgCO3 and MgO catalysts with nanosheet structures were also prepared by calcining Mg5(CO3)4(OH)2 ·4H2O at different temperature. The samples were characterized by transmission electron microscopy (TEM), scanning electron microscopy (SEM), X-ray diffraction (XRD), N2 adsorption–desorption, Fourier transform infrared (FTIR) and differential thermal analysis–thermogravimetry (DTA–TG). It was found that all the Mg-based catalysts exhibited regular nanosheet structure with high surface area. Although all of them are efficient catalysts for the Baeyer–Villiger oxidation of cyclohexanone to the corresponding lactone with aqueous hydrogen peroxide as the green oxidant, the Mg5(CO3)4(OH)2 ·4H2O surpassed all of them and the catalytic activity ( are higher than those Mg-based catalysts reported by other groups. The higher surface area, the special nanosheet structure as well as the enriched OH− and species on the Mg5(CO3)4(OH)2 ·4H2O catalysts all account for its higher activity. [Copyright &y& Elsevier]

Abstract: Visible-light responsible N,S-codoped titania photocatalyst was fabricated by simple hydrolysis of titania tetrachloride using ammonia in the presence of glacial acetic acid and ammonium sulfate. The N,S-codoped titania materials were fabricated by a template-free route and demonstrated twist-like helix morphology. The morphology and microstructure characteristics of N,S-codoped titania photocatalysts were characterized by means of the N2 adsorption–desorption measurements, thermal gravimetric and differential thermal analysis (TG-DTA), transmission electron microscopy (TEM), scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS), Fourier transform infrared spectroscopy (FT-IR), UV–visible diffuse reflectance spectra (DRS) and X-ray powder diffraction (XRD). The unique morphology of N,S-codoped titania materials and mesoporous microstructure were maintained after a heat treatment at 723K for 3h, exhibiting significantly thermal stability. The photocatalytic activity was evaluated by degrading phenol in aqueous suspension under ultraviolet and visible light irradiation. The results obtained with these novel photocatalysts are compared with the behavior of the well-studied and widely used Degussa P25 TiO2 under the same conditions. The N,S-codoped titania samples were more superior than P25 and the sample calcined under 723K for 3h shows the best photocatalytic activity, the higher activity of which could be attributed to its high surface area, large pore volume, well-crystallized anatase, red-shift in adsorption edge and strong absorbance of light with longer wavelength. [Copyright &y& Elsevier]

Mouse skin tumorigenicity studies indicate that benzo[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE) contributes to carcinogenesis as both a tumor initiator and promoter. However, the mechanisms that mediate B[a]PDE tumor promotion effects remain unclear. Our results demonstrated that in mouse epidermal CI41 cells, B[a]PDE treatment resulted in marked activation of AP-1 and its upstream MAPKs, including ERKs, JNKs and p38K. B[a]PDE exposure also led to activation of phosphotidylinositol 3-kinase (PI-3K), Akt and p70 S6 kinase (p70S6k). B[a]PDE-induced AP-1 transactivation was inhibited by pretreatment of cells with PI-3K inhibitors, wortmannin or Ly294002. In contrast, inhibition of p70S6k with rapamycin did not show any inhibitory effects. An overexpression of dominant-negative mutant of PI-3K, Δp85, impaired B[a]PDE-induced activation of PI-3K, Akt and AP-1 transactivation. Furthermore, an overexpression of dominant-negative Akt mutant, Akt-T308A/S473A, blocked B[a]PDE-induced activation of Akt, AP-1 and JNKs, while it did not affect the activation of p70S6k, ERKs and p38 kinase. These results demonstrated that B[a]PDE was able to induce AP-1 transactivation and this AP-1 induction was specific through PI-3K/Akt/JNKs-dependent and p70S6k-independent pathways. This study also indicated that Akt-T308A/S473A blocks B[a]PDE-induced AP-1 activation specific through impairing JNK pathway. These findings will help us to understand the signal transduction pathways involved in the carcinogenic effects of B[a]PDE. [ABSTRACT FROM AUTHOR]

5-Methylchrysene has been found to be a complete carcinogen in laboratory animals. However, the tumor promotion effects of (±)-anti-5-methylchrysene-1,2 diol-3,4-epoxide (5-MCDE) remain unclear. In the present work, we found that 5-MCDE induced marked activator protein-1 (AP-1) activation in C141 cells. 5-MCDE also induced a marked activation of phosphatidylinositol 3-kinase (PI-3K). Inhibition of PI-3K impaired 5-MCDE--induced AP-1 transactivation, suggesting that P1-3 K is an upstream kinase involved in API activation by 5-MCDE. Furthermore, we found that Akt is a PI-3K downstream mediator for 5-MCDE- induced AP-1 transactivation, whereas another PI-3K down-stream kinase, p7OS6K, was not involved in AP-1 activation by 5-MCDE. Moreover, inhibition of Akt activation blocked 5-MCDE-induced activation of extracellular signal-regulated protein kinases (ERKs) and c-Jun NH2-terminal kinases (JNKs), whereas it did not affect p38k activation. Consistently, overexpression of a dominant-negative mutant of ERK2 or JNK1 blocked the AP-1 activation by 5-MCDE. These results demonstrate that 5-MCDE is able to induce AP-1 activation, and the AP-1 induction is specifically through a Pl-3K/Akt-dependent and p70S6K-independent pathway. [ABSTRACT FROM AUTHOR]

The transcription factor activator protein-1 (AP-1) has been implicated in a large variety of biological processes including cell differentiation, proliferation, apoptosis and oncogenic transformation. It is thought that the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 activity is because of the activation of the PKC/MAPK/AP-1 pathway, although the detailed molecular mechanism has not been fully characterized. The tyrosine kinases of epidermal growth factor receptor (EGFR) lie at the head of a complex of signal transduction cascade that modulates cell proliferation, survival, adhesion, migration and differentiation. Currently, little is known about whether EGFR or its tyrosine kinase is necessary for TPA-induced AP-1 activation. In the present study, we investigated this issue using a well-characterized mouse fibroblast B82 cell line, which is devoid of the EGFR, and its stable transfectants with either wild-type EGFR (B82L) or tyrosine kinase-deficient EGFR (mutation at Lys-721) (B82M721). We demonstrated that the TPA or epidermal growth factor (EGF) induced AP-1 activation in the B82L cells that express wild-type EGFR, but not in the B82 cell, whereas autophosphorylation at tyrosine1173 of EGFR in B82L cells was only induced by EGF, but not TPA. The expression of tyrosine kinase-deficient EGFR (mutation at Lys-721) (B82M721) resulted in deficiency of AP-1 induction in cellular response to EGF, while TPA treatment led to fully AP-1 activation. Furthermore, the mutation at Lys-721 of EGFR resulted in impairing of EGFR autophosphorylation at tyrosine1173 induced by EGF. Based on these results, we conclude that TPA-induced AP-1 activation requires the basal level-EGFR protein, but not EGFR tyrosine kinase and EGFR autophosphorylation at tyrosine1173, whereas both EGFR tyrosine kinase and EGFR autophosphorylation at Y1173 play a critical role in EGF-induced AP-1 activation.Oncogene (2003) 22, 211–219.... [ABSTRACT FROM AUTHOR]

Alcohol abuse is a risk factor for cancers of the gastrointestinal tract, and it also can precipitate psoriasis characterized by hyperproliferation of epidermal cells. Because these effects of alcohol may involve stimulation of cell growth, and ethanol (EtOH) was shown to enhance DNA synthesis in mouse fibroblasts and epidermal cells, we conducted a study to determine whether EtOH can also stimulate mitogenesis in human fibroblasts and keratinocytes. In keratinocytes, EtOH had no effects on mitogenesis after shorter (17-hr) treatments, but it partially prevented inhibition of DNA synthesis elicited by longer treatments (3-4 days) with 2 mM calcium (Ca2+), a differentiation-inducing agent. In contrast, treatment of serum-starved zinc-treated (40 μM) human skin fibroblasts with 50-60 mM EtOH for 17 hr resulted in increased DNA synthesis. EtOH-induced DNA synthesis was blocked by 1 mM EGTA, a specific Ca2+ chelator. Despite the presence of 1.8 mM Ca2+ in the cell culture medium, the addition of 1 mM extra Ca2+ (final concentration, 2.8 mM) for 17 hr induced DNA synthesis, presumably mediated by Ca2+ receptors. In eight independent human skin fibroblast lines examined, treatment with EtOH for 46 hr, but not for 17 hr, invariably enhanced the effects of Ca2+ on DNA synthesis, consistent with synergistic stimulation of cell proliferation by EtOH and Ca2+. Neomycin, a Ca2+ receptor agonist, and EtOH also exerted synergistic effects on DNA synthesis after longer (46-hr) treatments. In mouse NIH 3T3 fibroblasts, both EtOH- and Ca2+ -enhanced DNA synthesis after 17-hr treatment, but they stimulated cell proliferation only in combination. The results indicate that in human fibroblasts, EtOH can potentiate the longer-term effects of high concentrations of Ca2+ on DNA synthesis whereas, in keratinocytes, EtOH may inhibit Ca2+ -induced differentiation. [ABSTRACT FROM AUTHOR]

Simple Summary: Bladder cancer ranks fourth among the most prevalent cancers in men and is the most expensive cancer to treat on a per-patient basis. The muscle-invasive form of bladder cancer is one of the deadliest cancers, with a 5-year survival rate of only 6% in patients with distant metastasis. Effective therapeutic options remain few and far between. SNHG1 is a long non-coding RNA that is over-expressed in 95% of muscle-invasive bladder cancers. However, very little information is available about the role and mechanisms of SNHG1 in bladder tumor formation and progression. Here, we provide experimental evidence establishing that SNHG1 drives bladder cancer cell invasion and stem-cell-like behaviors through a specific signaling pathway. Our results reveal novel biomarkers predictive of the progression of muscle-invasive bladder cancer and potential new targets for therapeutic intervention. The stem-cell-like behavior of cancer cells plays a central role in tumor heterogeneity and invasion and correlates closely with drug resistance and unfavorable clinical outcomes. However, the molecular underpinnings of cancer cell stemness remain incompletely defined. Here, we show that SNHG1, a long non-coding RNA that is over-expressed in ~95% of human muscle-invasive bladder cancers (MIBCs), induces stem-cell-like sphere formation and the invasion of cultured bladder cancer cells by upregulating Rho GTPase, Rac1. We further show that SNHG1 binds to DNA methylation transferase 3A protein (DNMT3A), and tethers DNMT3A to the promoter of miR-129-2, thus hyper-methylating and repressing miR-129-2-5p transcription. The reduced binding of miR-129-2 to the 3′-UTR of Rac1 mRNA leads to the stabilization of Rac1 mRNA and increased levels of Rac1 protein, which then stimulates MIBC cell sphere formation and invasion. Analysis of the Human Protein Atlas shows that a high expression of Rac1 is strongly associated with poor survival in patients with MIBC. Our data strongly suggest that the SNHG1/DNMT3A/miR-129-2-5p/Rac1 effector pathway drives stem-cell-like and invasive behaviors in MIBC, a deadly form of bladder cancer. Targeting this pathway, alone or in combination with platinum-based therapy, may reduce chemoresistance and improve longer-term outcomes in MIBC patients. [ABSTRACT FROM AUTHOR]

An experimental wideband chaotic ground penetrating radar is proposed to locate underground pipes. A chaotic signal with a bandwidth of 1.56 GHz is utilized as the probe signal. The localization of the pipes is achieved by correlating the chaotic echo signal with its delayed duplicate and back-projection algorithm. Experimental results demonstrate that plastic pipe, metallic pipe, and multiple pipes can be located with a range resolution of 10 cm. Limited by the height of the sand, the detectable range is estimated to be 0.7 m for both the plastic pipes and the metallic pipes when the transmitting power is −12 dBm. The proposed system has the potential to detect buried pipes, and it is suitable for geological and civil engineering applications. [ABSTRACT FROM AUTHOR]

Bladder cancer, the most common malignancy of the urinary tract, has a poor overall survival rate when the tumor becomes muscle invasive. The discovery and evaluation of new alternative medications targeting high-grade muscle invasive bladder cancer (MIBC) are of tremendous importance in reducing bladder cancer mortality. Isorhapontigenin (ISO), a stilbene derivative from the Chinese herb Gnetum cleistostachyum, exhibits a strong anti-cancer effect on MIBCs. Here, we report the whole transcriptome profiling of ISO-treated human bladder cancer T24 cells. A total of 1047 differentially expressed genes (DEGs) were identified, including 596 downregulated and 451 upregulated genes. Functional annotation and pathway analysis revealed that ISO treatment induced massive changes in gene expression associated with cell movement, migration, invasion, metabolism, proliferation, and angiogenesis. Additionally, ISO treatment-activated genes involved in the inflammatory response but repressed genes involved in hypoxia signaling, glycolysis, the actin cytoskeleton, and the tumor microenvironment. In summary, our whole transcriptome analysis demonstrated a shift in metabolism and altered actin cytoskeleton in ISO-treated T24 cells, which subsequently contribute to tumor microenvironment remodeling that suppresses tumor growth and progression. [ABSTRACT FROM AUTHOR]

Background: Immunochromatographic strips (ICSs) are a practical tool commonly used in point-of-care testing (POCT) applications. However, ICSs that are currently available have low sensitivity and require expensive equipment for quantitative analysis. These limitations prohibit their extensive use in areas where medical resources are scarce. Methods: We developed a novel POCT platform by integrating a gas generation biosensor with Au@Pt Core/Shell nanoparticle (Au@PtNPs)-based ICSs (G-ICSs). The resulting G-ICSs enabled the convenient and quantitative assessment of a target protein using the naked eye, without the need for auxiliary equipment or complicated computation. To assess this platform, C-reactive protein (CRP), a biomarker commonly used for the diagnosis of acute, infectious diseases was chosen as a proof-of-concept test. Results: The linear detection range (LDR) of the G-ICSs for CRP was 0.05–6.25 μg/L with a limit of detection (LOD) of 0.041 μg/L. The G-ICSs had higher sensitivity and wider LDR when compared with commonly used AuNPs and fluorescent-based ICSs. When compared with results from a chemiluminescent immunoassay, G-ICS concordance rates for CRP detection in serum samples ranged from 93.72 to 110.99%. Conclusions: These results demonstrated that G-ICSs have wide applicability in family diagnosis and community medical institutions, especially in areas with poor medical resources. [ABSTRACT FROM AUTHOR]

Emerging evidence has indicated that long non-coding RNAs (lncRNAs) play critical roles in tumor development and progression. Recent studies reported that lncRNA MIR22HG could play important roles in hepatocellular carcinoma and lung cancer progression. However, the expression and underlying mechanism of MIR22HG in endometrial cancer (EC) remain unclear. In the present study, qRT-PCR showed that MIR22HG expression was significantly downregulated in EC tissues. In vitro function assays showed that increased MIR22HG expression significantly inhibited EC cells proliferation, induced EC cells apoptosis, and arrested EC cells in G0/G1 phase. Furthermore, miR-141-3p was identified and confirmed to be the target of MIR22HG. Subsequently, DAPK1 was confirmed to be regulated by MIR22HG and miR-141-3p, and could play a positive role in inhibiting EC cells proliferation. Collectively, these data demonstrated that lncRNA MIR22HG could act as a tumor suppressor and inhibited EC cells proliferation through regulating miR-141-3p/DAPK1 axis, which provides a new therapeutic target for EC treatment. [ABSTRACT FROM AUTHOR]

Insulin-like growth factor binding protein-related protein 1 (IGFBP-rP1) is a potential tumor suppressor gene in a variety of cancers including colorectal cancer and breast cancer. However, its role and the potential mechanism in endometrial carcinoma (EC) are still unclear. The purpose of this study was to explore the effect of IGFBP-rP1 on EC cell proliferation and apoptosis and its underlying mechanism. Western blot analysis and reverse transcription-quantitative PCR were used to assess protein and gene expression levels of IGFBP-rP1 in EC cells. Overexpression of IGFBP-rP1 and/or AKT serine/threonine kinase was used to analyze their effects on cell proliferation and apoptosis of the EC cells. Co-immunoprecipitation and glutathione S transferase pull-down assays were used to analyze the interaction between IGFBP-rP1 and AKT. The expression of IGFBP-rP1 in EC cells was downregulated. Overexpression of IGFBP-rP1 inhibited the proliferation and induced apoptosis of EC cells, which were abolished by the overexpression of AKT. In addition, IGFBP-rP1 directly interacted with AKT to inhibit PI3K/AKT signaling. Additionally, M0 macrophages were induced by EC cells to differentiate into M2 macrophages, which was reversed by IGFBP-rP1. Overexpression of AKT in EC cells abolished the inhibitory effect of IGFBP-rP1 on M2 polarization. IGFBP-rP1 as an oncogenic factor inhibits M2 polarization of TAMs through PI3K/AKT signaling pathway and may be a potentially valuable target for EC therapy. [ABSTRACT FROM AUTHOR]

Ground-penetrating radar (GPR) is an effective geophysical electromagnetic method for underground target detection. However, the target response is usually overwhelmed by strong clutter, thus damaging the detection performance. To account for the nonparallel case of the antennas and the ground surface, a novel GPR clutter-removal method based on weighted nuclear norm minimization (WNNM) is proposed, which decomposes the B-scan image into a low-rank clutter matrix and a sparse target matrix by using a non-convex weighted nuclear norm and assigning different weights to different singular values. The WNNM method's performance is evaluated using both numerical simulations and experiments with real GPR systems. Comparative analysis with the commonly used state-of-the-art clutter removal methods is also conducted in terms of the peak signal-to-noise ratio (PSNR) and the improvement factor (IF). The visualization and quantitative results demonstrate that the proposed method outperforms the others in the nonparallel case. Moreover, it is about five times faster than the RPCA, which is beneficial for practical applications. [ABSTRACT FROM AUTHOR]

A direct chaotic through-wall imaging (TWI) radar using chaotic signal generated by improved Colpitts oscillator is proposed, and its good anti-jamming performance is investigated theoretically and experimentally. Compared with conventional TWI radar, the proposed radar has the advantages of very high range resolution, low probability of intercept, and immunity from jamming and interference. The characteristics of the chaotic signal are presented. According to the delta function-like autocorrelation of the chaotic signal, the range resolution of the radar is 6 cm. The cross-ambiguity functions with no discernible peaks are used to theoretically certify its interference immunity performance, and then the anti-jamming properties in the Colpitts jamming, linear frequency modulated chirp jamming, and noise jamming environments are demonstrated by numerical electromagnetic simulations using finite difference time domain, and the corresponding experiments. The simulation and experimental results show that the chaotic waveform possesses excellent jamming immunity to the noise and radio frequency interference. This feature makes the chaotic signal perform superbly in multi-radar environments. [ABSTRACT FROM AUTHOR]

Simple Summary: Lung adenocarcinoma (LUAD) has a high mortality and incidence rate. The therapeutic efficacy of LUAD varies with the individual heterogeneity of the tumor microenvironment (TME). It is necessary to explore more biomarkers and targets to improve the prognosis of patients. Ubiquitination pathways are involved in the biological process of regulating the anti-tumor immunity of immune cells and immunosuppression of tumor cells in the TME of patients. In this study, we clarified the characteristics of ubiquitin-related gene pairs (UbRGPs) and identified the relationship between the status of the TME and UbRGPs of patients with LUAD. A prognostic signature based on six UbRGPs was established, which performed well in predicting the immune infiltration and tumor mutation burden (TMB) in the TME and the response of LUAD to immuno-, chemo-, and targeted therapy. In conclusion, the UbRGPs signature is an independent prognostic indicator and has great potential in assisting the clinical therapy for patients with LUAD. Lung adenocarcinoma (LUAD) is a common pathological type of lung cancer worldwide, and new biomarkers are urgently required to guide more effective individualized therapy for patients. Ubiquitin-related genes (UbRGs) partially participate in the initiation and progression of lung cancer. In this study, we used ubiquitin-related gene pairs (UbRGPs) in tumor tissues to access the function of UbRGs in overall survival, immunocyte infiltration, and tumor mutation burden (TMB) of patients with LUAD from The Cancer Genome Atlas (TCGA) database. In addition, we constructed a prognostic signature based on six UbRGPs and evaluated its performance in an internal (TCGA testing set) and an external validation set (GSE13213). The prognostic signature revealed that risk scores were negatively correlated with the overall survival, immunocyte infiltration, and expression of immune checkpoint inhibitor-related genes and positively correlated with the TMB. Patients in the high-risk group showed higher sensitivity to partially targeted and chemotherapeutic drugs than those in the low-risk group. This study contributes to the understanding of the characteristics of UbRGPs in LUAD and provides guidance for effective immuno-, chemo-, and targeted therapy. [ABSTRACT FROM AUTHOR]

In order to prevent illegal intrusion, theft, and destruction, important places require stable and reliable human intrusion detection technology to maintain security. In this paper, a combined sensing system using anti-jamming random code signals is proposed and demonstrated experimentally to detect the human intruder in the protected area. This sensing system combines the leaky coaxial cable (LCX) sensor and the single-transmitter-double-receivers (STDR) radar sensor. They transmit the orthogonal physical random code signals generated by Boolean chaos as the detection signals. The LCX sensor realizes the early intrusion alarm at the protected area boundary by comparing the correlation traces before and after intrusion. Meanwhile, the STDR radar sensor is used to track the intruder's moving path inside the protected area by correlation ranging and ellipse positioning, as well as recognizing intruder's activities by time-frequency analysis, feature extraction, and support vector machine. The experimental results demonstrate that this combined sensing system not only realizes the early alarm and path tracking for the intruder with the 13 cm positioning accuracy, but also recognizes the intruder's eight activities including squatting, picking up, jumping, waving, walking forward, running forward, walking backward, and running backward with 98.75% average accuracy. Benefiting from the natural randomness and auto-correlation of random code signal, the proposed sensing system is also proved to have a large anti-jamming tolerance of 27.6 dB, which can be used in the complex electromagnetic environment. [ABSTRACT FROM AUTHOR]

Abstract: Suberoylanilide hydroxamic acid (SAHA) inhibiting cancer cell growth has been associated with its downregulation of cyclin D1 protein expression at transcription level or translation level. Here, we have demonstrated that SAHA inhibited EGF-induced Cl41 cell transformation via the decrease of cyclin D1 mRNA stability and induction of G0/G1 growth arrest. We found that SAHA treatment resulted in the dramatic inhibition of EGF-induced cell transformation, cyclin D1 protein expression and induction of G0/G1 growth arrest. Further studies showed that SAHA downregulation of cyclin D1 was only observed with endogenous cyclin D1, but not with reconstitutionally expressed cyclin D1 in the same cells, excluding the possibility of SAHA regulating cyclin D1 at level of protein degradation. Moreover, SAHA inhibited EGF-induced cyclin d1 mRNA level, whereas it did not show any inhibitory effect on cyclin D1 promoter-driven luciferase reporter activity under the same experimental conditions, suggesting that SAHA may decrease cyclin D1 mRNA stability. This notion was supported by the results that treatment of cells with SAHA decreased the half-life of cyclin D1 mRNA from 6.95h to 2.57h. Consistent with downregulation of cyclin D1 mRNA stability, SAHA treatment also attenuated HuR expression, which has been well-characterized as a positive regulator of cyclin D1 mRNA stability. Thus, our study identifies a novel mechanism responsible for SAHA inhibiting cell transformation via decreasing cyclin D1 mRNA stability and induction of G0/G1 growth arrest in Cl41 cells. [Copyright &y& Elsevier]

Background: Hexavalent chromium [Cr(VI)] is recognized as a human carcinogen via inhalation. However, the molecular mechanisms by which Cr(VI) causes cancers are not well understood. Objectives: We evaluated cyclooxygenase-2 (COX-2) expression and the signaling pathway leading to this induction due to Cr(VI) exposure in cultured cells. Methods: We used the luciferase reporter assay and Western blotting to determine COX-2 induction by Cr(VI). We used dominant negative mutant, genetic knockout, gene knockdown, and chromatin immunoprecipitation approaches to elucidate the signaling pathway leading to COX-2 induction. Results: We found that Cr(VI) exposure induced COX-2 expression in both normal human bronchial epithelial cells and mouse embryonic fibroblasts in a concentration- and time-dependent manner. Deletion of IKKβ [inhibitor of transcription factor NFκB (IκB) kinase β; an upstream kinase responsible for nuclear factor κB (NFκB) activation] or overexpression of TAM67 (a dominant-negative mutant of c-Jun) dramatically inhibited the COX-2 induction due to Cr(VI), suggesting that both NFκB and c-Jun/AP-1 pathways were required for Cr(VI)-induced COX-2 expression. Our results show that p65 and c-Jun are two major components involved in NFκB and AP-1 activation, respectively. Moreover, our studies suggest crosstalk between NFκB and c-Jun/AP-1 pathways in cellular response to Cr(VI) exposure for COX-2 induction. Conclusion: We demonstrate for the first time that Cr(VI) is able to induce COX-2 expression via an NFκB/c-Jun/AP-1-dependent pathway. Our results provide novel insight into the molecular mechanisms linking Cr(VI) exposure to lung inflammation and carcinogenesis. [ABSTRACT FROM AUTHOR]

It is well-known that insoluble nickel compounds possess much more potent carcinogenic activities as compared with soluble nickel compounds. Although it is assumed that the different entry and clearance rate are responsible for the difference, the mechanisms underlying the different carcinogenic activities are still not well understood yet. In the present study, we found that exposure to soluble, but not insoluble nickel compounds, caused a significant inhibition of cell growth and G1/G0 cell cycle arrest, which was concomitant with a marked down-regulation of cylin D1, an essential nuclear protein for controlling G1/S transition, while both soluble and insoluble nickel compounds showed similar effects on NFκB activation, HIF-1α protein accumulation and TNF-α transcription and CAP43 protein expression at same doses range. The down-regulation of cyclin D1 is due to protein degradation rather than inhibition of transcription, because the nickel compounds treatment did not change cyclin D1 mRNA level, while MG132, the proteasome inhibitor, can rescue the degradation of cyclin D1 caused by soluble nickel compound. Moreover, the soluble nickel-induced cyclin D1 degradation is dependent on its Thr286 residue and requires IKKα, but not HIF-1α, which are both reported to be involved in cyclin D1 down-regulation. Taken together, we demonstrate that soluble, but not insoluble nickel compound, is able to cause cyclin D1 degradation and a cell growth arrest in an IKKα-dependent manner. Given the role of cyclin D1 and cell proliferation in carcinogenesis, we anticipate that the different effects of soluble and insoluble nickel compounds on cyclin D1 degradation and cell growth arrest may at least partially account for their different carcinogenic activities. J. Cell. Physiol. 218: 205–214, 2009. © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Abstract: Thermally stable mesoporous core-shell structured nanocrystallite titanium dioxide (TiO2) microspheres were prepared by a novel hydro-alcohol thermal method. Anatase powders were synthesized under hydrothermal condition at 368K from aqueous titania tetrachloride solution with the presence of urea and ammonium sulfate, then the samples were annealed at various temperatures before testing their photocatalytic activity. The morphology and microstructure characteristics of TiO2 microspheres series were characterized by means of the specific surface area (BET), transmission electron microscopy (TEM), scanning electron microscopy (SEM), differential thermal analysis (DTA), photoluminescence spectra (PLS), X-ray photoelectron spectroscopy (XPS) and X-ray powder diffraction (XRD). The specific microsphere structures were maintained after a heat treatment at 973K for 3h, exhibiting a significant thermal stability. The photocatalytic activity was measured in a reactor with ultraviolet lamps. The catalysts show considerably high catalytic activity and recyclability during the photodegradation of phenol in aqueous suspension, the microsphere titania sample calcinated under 733K for 3h shows the best photocatalytic activity. The results obtained with this novel photocatalyst are compared with the behavior of the well-studied and widely used Degussa P25 TiO2 under the same conditions. [Copyright &y& Elsevier]

Abstract: Apertured N-doped TiO2 microtubes have been fabricated by simple hydrolysis of titania tetrachloride using ammonia without any external templates. The morphology and microstucture characteristics of apertured N-doped TiO2 microtubes were characterized by means of the specific surface area (BET), transmission electron microscopy (TEM), scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS), Fourier transformed infrared (FT-IR), UV–visible diffuse reflectance spectra (DRS) and X-ray powder diffraction (XRD). The unique morphology of microtubes and mesoporous microstructure were maintained after a heat treatment at 723K for 3h, exhibiting significantly thermal stability. The catalysts exhibited high ultraviolet and visible light photocatalytic activity in degrading phenol and methyl orange. [Copyright &y& Elsevier]

Abstract: A La-doped TiO2(La/TiO2) photocatalyst with optimum La/Ti molar ratio of 1.25% is prepared by ultrasound-assisted sol–gel method, followed by supercritical drying in ethanol fluid. During liquid phase photocatalytic degradation of phenol, the as-prepared La/TiO2 exhibits higher activity than the La/TiO2 obtained without ultrasonication. Meanwhile, the La/TiO2 obtained via supercritical treatment is more active than either the undoped TiO2 obtained under supercritical conditions or the La/TiO2 obtained via direct calcination instead of supercritical treatment. Based on various characterizations, the promoting effects of ultrasonication, supercritical treatment, and La-modification are discussed by considering the enhanced particle dispersion, the higher crystallization degree of anatase and the increase of the surface oxygen vacancies and/or defects, which facilitates the adsorption of phenol molecules and also inhibits the recombination between photoelectrons and holes, resulting in the higher quantum efficiency of photocatalysis. Meanwhile, the ultrasonication and supercritical treatment also strengthen the interaction between the La-dopants and the TiO2, which could enhance the light absorbance and thus, increase the photocatalytic activity. [Copyright &y& Elsevier]

Recent studies from our laboratory have shown that the transactivation of nuclear factor κ B (NFκ B) and activator protein-1 (AP-1) plays an important mechanistic role in ultraviolet (UV)-induced skin carcinogenesis in mice. We also demonstrated that a methanol extract (ME) fraction from black raspberries (Rubus occidentalis) (RO; RO-ME) inhibits benzo[a]pyrene-7,8-diol-9,10-epoxide [B(a)PDE]—induced activation of NFκ B and AP-1 in cultured mouse epidermal cells. In the present study, we determined if RO-ME might also inhibit the induction of NFκ B and AP-1 in mouse epidermal cells exposed to mid UV radiation (UVB) and short UV radiation (UVC) and whether methanol fractions from strawberries and blueberries would also be effective. Our results showed that RO-ME inhibited UVB-induced activation of NFκ B in mouse epidermal cells in a time- and dose-dependent manner; however, the methanol fractions from strawberries and blueberries were ineffective. Interestingly, none of the fractions from all 3 berry types inhibited UVB- or UVC-induced activation of AP-1, suggesting that inhibition of UV-induced signaling pathways is specific for black raspberries and NFκ B. Cyanidin-3-rutinoside, an anthocyanin found in abundance in black raspberries and not in strawberries or high-bush blueberries, was found to contribute to the inhibition of UVB-induced activation of NFκ B. These results suggest that berries differ in their ability to influence signaling pathways leading to activation of NFκ B and AP-1 when using UV light as the inducer. [ABSTRACT FROM AUTHOR]

Epithelial mesenchymal transition (EMT) is highly correlated with metastasis during cancer development. Although previous studies have revealed that ISO is able to inhibit cancer cell invasion and stem-cell properties, little is known about the effects of ISO on EMT markers. The present study explores the potential regulation of ISO on EMT, leading to the inhibition of migration and invasion of bladder cancer cells. We found that ISO inhibited Vimentin, one of the EMT markers, in the invasive bladder cancer cell lines U5637 and T24T. ISO reduced Vimentin protein level by increasing the expression of METTL14. On the other hand, ISO upregulated the METTL14 mRNA by activating the transcription factor FOXO3a. The results demonstrate that ISO inhibits invasion by affecting the EMT marker and offer a novel insight into understanding the upregulation of METTL14 by ISO. • The effect on EMT and its potential mechanisms of ISO is first explored. • ISO treatment significantly upregulated the protein expression of METTL14 via activating its promoter. • ISO treatment inhibited the Vimentin expression by increasing the expression of METTL14. • The study of the effect on anti-cancer by ISO provides novel insight against BC. [ABSTRACT FROM AUTHOR]

Epithelial mesenchymal transition (EMT) is highly correlated with metastasis during cancer development. Although previous studies have revealed that ISO is able to inhibit cancer cell invasion and stem-cell properties, little is known about the effects of ISO on EMT markers. The present study explores the potential regulation of ISO on EMT, leading to the inhibition of migration and invasion of bladder cancer cells. We found that ISO inhibited Vimentin, one of the EMT markers, in the invasive bladder cancer cell lines U5637 and T24T. ISO reduced Vimentin protein level by increasing the expression of METTL14. On the other hand, ISO upregulated the METTL14 mRNA by activating the transcription factor FOXO3a. The results demonstrate that ISO inhibits invasion by affecting the EMT marker and offer a novel insight into understanding the upregulation of METTL14 by ISO. [ABSTRACT FROM AUTHOR]

Immune cell therapy presents a paradigm for the treatment of malignant tumors. Human Vγ9Vδ2 T cells, a subset of peripheral γδ T cells, have been shown to have promising anti-tumor activity. However, new methodology on how to achieve a stronger anti-tumor activity of Vγ9Vδ2 T cells is under continuous investigation. In this work, we used selenium nanoparticles (SeNPs) to strengthen the anti-tumor cytotoxicity of Vγ9Vδ2 T cells. We found SeNPs pretreated γδ T cells had significantly stronger cancer killing and tumor growth inhibition efficacy when compared with γδ T cells alone. Simultaneously, SeNPs pretreatment could significantly upregulate the expression of cytotoxicity related molecules including NKG2D, CD16, and IFN-γ, meanwhile, downregulate PD-1 expression of γδ T cells. Importantly, we observed that SeNPs promoted tubulin acetylation modification in γδ T cells through interaction between microtubule network and lysosomes since the latter is the primary resident station of SeNPs shown by confocal visualization. In conclusion, SeNPs could significantly potentiate anti-tumor cytotoxicity of Vγ9Vδ2 T cells, and both cytotoxicity related molecules and tubulin acetylation were involved in fine-tuning γδ T cell toxicity against cancer cells. Our present work demonstrated a new strategy for further enhancing anti-tumor cytotoxicity of human Vγ9Vδ2 T cells by using SeNPs-based nanotechnology, not gene modification, implicating SeNPs-based nanotechnology had a promising clinical perspective in the γδ T cell immunotherapy for malignant tumors. [ABSTRACT FROM AUTHOR]

We present a chaotic lidar for underwater ranging and three-dimension (3D) imaging applications. The lidar transmitter based on a laser diode with free space optical feedback is designed to generate 520 nm wavelength wideband chaotic signal. This transmitter is used with a correlation-based lidar receiver to perform a ranging demonstration in clean water with a measured attenuation coefficient of 0.06 m−1 at 520 nm. The experimental results prove that 1.2 cm mean absolute error (MAE) and 3.4 cm range resolution can be achieved and kept in a range of 140 cm at least. Moreover, employing a two-axis mirror for laser scanning, the possibility of the designed chaotic lidar system for 3D imaging is also verified. [ABSTRACT FROM AUTHOR]

Cancer stem cells (CSC) are highly associated with poor prognosis in cancer patients. Our previous studies report that isorhapontigenin (ISO) down-regulates SOX2-mediated cyclin D1 induction and stem-like cell properties in glioma stem-like cells. The present study revealed that ISO could inhibit stem cell-like phenotypes and invasivity of human bladder cancer (BC) by specific attenuation of expression of CD44 but not SOX-2, at both the protein transcription and degradation levels. On one hand, ISO inhibited cd44 mRNA expression through decreases in Sp1 direct binding to its promoter region-binding site, resulting in attenuation of its transcription. On the other hand, ISO also down-regulated USP28 expression, which in turn reduced CD44 protein stability. Further studies showed that ISO treatment induced miR-4295, which specific bound to 3′-UTR activity of usp28 mRNA and inhibited its translation and expression, while miR-4295 induction was mediated by increased Dicer protein to enhance miR-4295 maturation upon ISO treatment. Our results provide the first evidence that ISO has a profound inhibitory effect on human BC stem cell-like phenotypes and invasivity through the mechanisms distinct from those previously noted in glioma stem-like cells. [ABSTRACT FROM AUTHOR]

Background: Cholangiocarcinoma (CCA) is a highly aggressive and fatal tumor. CCA occurs in the epithelial cells of bile ducts. Due to increasing incidences, CCA accounts for 3% of all gastrointestinal malignancies. In addition to comprehensive treatments for cancer, such as surgery, chemotherapy, and radiotherapy, during the past few years, cellular immunotherapy has played an increasingly important role. As a result of our research, we have discovered the γδ T cell-based immunotherapy for CCA. Case presentation: A 30-year-old male (https://www.clinicaltrials.gov/ ID: NCT02425735) was diagnosed with recurrent mediastinal lymph node metastasis after liver transplantation because of Cholangiocarcinoma (stage IV). In the course of his therapy sessions, he only received allogenic γδ T cell immunotherapy from August, 2017 through February, 2018 (8 infusions in total). γδ T cells were expanded from peripheral blood mononuclear cells (PBMCs) of healthy donor, and ~ 4 × 108 cells were adoptive transferred to the patient. Conclusion: In the above case report of the Cholangiocarcinoma (stage IV) patient who had received liver transplantation and afterward was diagnosed with recurrent mediastinal lymph node metastasis, we clinically proved that allogenic γδ T cell treatment had no adverse effects. We observed that allogenic γδ T cell treatments positively regulated peripheral immune functions of the patient, depleted tumor activity, improved quality of life, and prolonged his life span. After 8 γδ T cell treatments, the size of lymph nodes was remarkably reduced with activity depletion. This clinical work suggested that allogenic γδ T cell immunotherapy could be developed into a promising therapy drug for CCA. [ABSTRACT FROM AUTHOR]